Surfactant protein-A (SP-A) is a collectin protein found in airway epithelia that plays an important role in modulating both innate and adaptive defence against inhaled pathogens. This review emphasises the correlations of altered SP-A function in asthma and chronic rhinosinusitis, as well as its potential relevance as a targeted treatment for sinusitis. SP-A has been found to bind and opsonize inhaled pathogens, allowing germs to be cleared by phagocytosis. The researchers recently discovered that Pseudomonas aeruginosa, a frequent bacterial culprit in chronic rhinosinusitis, raises SP-A levels. Furthermore, SP-A has been found to alter epithelial inflammatory mediators as well as play a role in eosinophil-mediated airway illness. The construction of a transgenic mouse model expressing human SP-A2 genetic variations has revealed that the human surfactant protein-A2 223K mutation dramatically promotes eosinophil degranulation, implying a genotype-phenotype association in human airway illness.

SP-A has a role in both innate and adaptive host defence systems in the upper and lower airways. Although research in this topic in sinusitis is still in its early stages, preliminary findings show that abnormal SP-A regulation may be one of the etiologic factors in the development of bacterial and eosinophilic sinusitis.